Delayed development of humoral immunity in chickens following in ovo treatment with mibolerone

In order to determine if mibolerone causes rapid development of the humoral immune system as previously hypothesized, 12-day-old chicken embryos were injected with 0.1, 1, or 10 micrograms mibolerone. Mibolerone caused bursal atrophy in a dose-dependent manner with severe atrophy at the 10 micrograms dose, substantial atrophy at the 1 microgram dose, and very little or no atrophy at the 0.1 microgram dose. Mibolerone-treated chicks were subsequently challenged with sheep red blood cells (SRBC) and Brucella abortus at 1, 7, 14, or 21 days of age. When serum samples were analysed for agglutinins to SRBC and B. abortus, the results indicated that treated chickens had lower agglutinin titers to both antigens at younger ages. These responses improved with age in groups treated with 0.1 microgram and 1 microgram and were comparable to controls at 5 weeks of age except for low primary and secondary (IgG specific) titers to B. abortus in birds treated with 1 microgram. Chickens treated with 10 micrograms mibolerone still had considerably lower primary responses to SRBC and lower primary as well as secondary responses to B. abortus at 4 and 5 weeks of age. These results indicate that mibolerone causes delayed rather than rapid development of the humoral immune system. In control as well as in treated chickens, agglutinin responses to SRBC appeared earlier than responses to B. abortus.     

Unruptured sinus of Valsalva aneurysm mimicking as right atrial tumor

Sinus of Valsalva aneurysm is a rare congenital cardiac abnormality and is usually diagnosed when it ruptures. An asymptomatic 55‐year‐old male of unruptured sinus of Valsalva aneurysm of noncoronary cusp was on medical follow‐up. At 2‐year follow‐up, there was thrombus formation in the aneurysm, mimicking right atrium tumor on 2D transthoracic echocardiography. Cardiac computed tomography showed filling defect in the aneurysm suggestive of thrombus. Considering the high risk of systemic emboli surgery was performed, and aneurysm was repaired with Dacron patch.     

Transcatheter Retrieval of Embolized AMPLATZER Septal Occluder

In selected patients, transcatheter closure of atrial septal defects with the AMPLATZER Septal Occluder has yielded excellent results. However, there is a slight risk of device embolization after deployment. We report the case of a 26-year-old woman in whom an embolized AMPLATZER device was retrieved percutaneously from the right pulmonary artery. We also discuss important technical principles for managing this uncommon but potentially severe complication.Key words: Device removal/methods, embolization, therapeutic/instrumentation, heart catheterization/instrumentation, heart septal defects, atrial/ultrasonography, patient selection, prosthesis implantation/adverse effects, prostheses and implants, septal occluder device/adverse effects, treatment outcomeTranscatheter closure of atrial septal defects (ASDs) with use of the AMPLATZER® Septal Occluder (St. Jude Medical, Inc.; St. Paul, Minn) has yielded excellent results in properly selected patients.^1,2 The major advantage of the AMPLATZER occluder is its easy retrieval at all stages of deployment before its final release from the delivery cable. Although embolization of AMPLATZER ASD occluders is rare, it can occur even when interventional cardiologists are experienced. Despite an earlier belief that the transcatheter retrieval of embolized AMPLATZER devices would be difficult, success rates from 50% to 75% have been reported.^3,4 We describe the retrieval of an embolized AMPLATZER device in a young woman. In addition, we present some technical principles with which operators practicing device closure should be familiar.     

The effects of in ovo mibolerone treatment on the bursa of Fabricius and the humoral system of chickens: a dose-response study

The effects of various doses of mibolerone, an analog of testosterone, in the development of the bursa of Fabricius and the humoral immune system were examined by injecting 0.01, 0.1, 1, 10 or 100 micrograms mibolerone into the chorio-allantoic cavity of 12-day-old chick embryos. Treatment with 0.01 or 0.1 micrograms of mibolerone caused slight or no bursal atrophy, 1 microgram caused substantial bursal atrophy, and 10 or 100 micrograms caused severe bursal atrophy at the time of hatching and at 6 weeks of age. When mibolerone-treated birds were challenged with sheep red blood cells and killed Brucella abortus at 4 and 5 weeks of age, birds treated with 10 or 100 micrograms of mibolerone had suppressed humoral responses to sheep erythrocytes and B. abortus whereas birds treated with 0.01 and 0.1 micrograms of mibolerone had normal humoral immune responses. Birds treated with 1 microgram mibolerone had normal humoral immune responses to sheep erythrocytes and B. abortus (except for low IgG responses to B. abortus) despite the fact that the birds had substantially atrophic bursae during their embryonic and post-embryonic development. These results are discussed in relation to an earlier claim that mibolerone given in microgram quantities in feed during the post-hatch period causes rapid development of the humoral immune system.     

The evaluation and management of patients with neuroleptic malignant syndrome

NMS is a rare but fatal syndrome that needs to be considered in the perioperative period. Although many aspects remain unexplored and controversial, with greater awareness of the condition, new concepts are coming into light. Definitive treatment guidelines remain an important issue to be addressed. Efforts have been initiated in that direction and all cases can be reported on a toll-free hotline ( 1-888-667-8367) or online (www.nmsis.org).     

A critical role for matrix metalloproteinases in liver regeneration

BACKGROUND: Matrix metalloproteinases (MMPs), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) are mediators of liver regeneration. To determine whether MMPs are required for normal hepatic regeneration, we performed 67% hepatectomies on mice treated with a broad-spectrum MMP-inhibitor, and assessed the effect on liver regeneration and urinary MMP activity. METHODS: Mice were subjected to sham operations, 67% hepatectomy, or 67% hepatectomy plus treatment with the broad-spectrum MMP inhibitor Marimastat. Urine collected preoperatively and for 8 d postoperatively was tested for MMP-2 and MMP-9 activity using zymography. Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, bilirubin, TNF-alpha, IL-6, and hepatocyte growth factor levels were measured. Liver sections were analyzed by CD31 immunohistochemistry and microvessel density. Mitotic index and proliferating cell nuclear antigen labeling index were determined. RESULTS: The mean regenerating liver weight on postoperative day 8 was 0.72 +/- 0.01 grams for the hepatectomy Marimastat group, and 0.83 +/- 0.02 grams for the hepatectomy control group (P < 0.001). Urinary MMP-9 activity was elevated during hepatic regeneration, and decreased on postoperative day 8 when the liver returned to its preoperative mass. In contrast, urine from hepatectomy Marimastat mice, in which liver regeneration was successfully inhibited, showed consistently low levels of MMP-2 and MMP-9 activity. The hepatectomy Marimastat group also exhibited elevated serum IL-6 levels on post-operative day 8, while serum TNF-alpha soluble receptor II levels were unchanged. Hepatocyte growth factor levels were not significantly different between the control hepatectomy and hepatectomy Marimastat groups at days 2, 4, and 8. Liver microvessel density was reduced in the hepatectomy Marimastat group at day 4. Mitotic index and proliferating cell nuclear antigen index were significantly decreased in the Marimastat hepatectomy group at post-operative day 2. CONCLUSIONS: The broad-spectrum MMP-inhibitor Marimastat inhibits liver regeneration. Microvessel density is reduced at day 4. Furthermore, urinary MMP-9 is elevated during liver regeneration, and this effect is not observed when regeneration is inhibited by the broad-spectrum MMP-inhibitor Marimastat.